Neonatal infraorbital nerve transection in rat results in peripheral trigeminal sprouting

Retrograde tracing techniques were employed to determine whether transection of the infraorbital (IO) nerve in either newborn or adult rats resulted in peripheral sprouting by undamaged trigeminal (V) axons. The IO nerve was sectioned just behind the vibrissa pad, either on the day of birth or when animals reached at least 60 days of age. After an additional 60 days, the same nerve was retransected in the orbit; horseradish peroxidase (HRP) or diamidino yellow (DY) was injected into the central portion of the vibrissa pad; and animals were killed 2-3 days later. In the neonatally nerve-damaged rats, this procedure invariably labelled primary afferent neurons in both the ipsilateral and contralateral V ganglia. On the ipsilateral side, these cells were located in the caudal portion of the ophthalmic-maxillary region and, less often, in the mandibular division. Their average diameter was 22.6 micron (s.d. = 5.6). On the contralateral side, most labelled ganglion cells were visible in the anteromedial part of the ophthalmic-maxillary region but a few could also be seen in the mandibular division. Their average diameter was 21.1 micron (s.d. = 5.5). No labelled ganglion cells were observed in adult rats subjected to the same series of manipulations. In a separate series of neonatally nerve-damaged animals, the above-described procedures were combined with neonatal injection of capsaicin in an effort to determine whether the observed sprouting was dependent upon the presence of large numbers of unmyelinated axons. The addition of this treatment reduced the number of labelled cells in both the ipsilateral and contralateral ganglia, but it did not alter either their distribution or average soma diameter. In a final experiment, sequential double-labelling techniques were used to determine whether the V axons that projected to the vibrissa pad via non-IO nerve branches were the result of sprouting by undamaged ganglion cells or arose from neurons that had originally projected into the IO nerve, were axotomized by our lesions, and regenerated to the vibrissa pad via another V branch. Here, the long-lived retrograde tracer true blue (TB) was injected into the vibrissa pad 6-8 hours before the neonatal nerve cut and DY was deposited into the pad after transection of the regenerate IO nerve in adulthood. Double-labelled cells in this experiment would have projected to the vibrissa pad via the IO nerve at birth and regenerated to it via another V branch in adulthood. Nearly 55% of the DY-labelled cells in this experiment also contained TB.(ABSTRACT TRUNCATED AT 400 WORDS)     

Brainstem and spinal projections of the deep cerebellar nuclei in the monkey,with observations on the brainstem projections of the dorsal column nuclei

Miniature end-plate potentials (MEPPs) recorded at the neuromuscular junction were initially reported to be normally distributed and have been attributed to quantal ACh release. This quantum was later correlated with the release of the content of one clear vesicle. This is the ‘classical vesicular hypothesis’. Recent observations of subminiature end-plate potentials (s-MEPPs) and of multimodal distribution of the MEPP amplitudes have led to the formulation of a new 'multivesicular hypothesis'. It attributes the s-MEPP to the release of one vesicle and the MEPP to the simultaneous release of several vesicles at one active zone.The distribution of MEPP intervals, the evaluation of the ACh content of a vesicle and of the ACh necessary to produce a MEPP, estimates of the number of vesicles missing following repeated stimulation, and the freeze fracture studies of the active zone do not permit a definitive rejection of either hypotheses.     

A comparison of the effects of two antispastic drugs,tizanidine and baclofen,on synaptic transmission from muscle spindle afferents to spinal interneurones in cats

The α₂-adrenergic agonist tizanidine was reported to be more efficient than baclofen in reducing muscle tone in some spastic patients. The aim of this study was to investigate if this might be due to more specific depressive actions of tizanidine on transmission from muscle afferents which contribute to muscle tone. This was done by comparing the effects of tizanidine and baclofen on amplitudes of monosynaptic spinal focal field potentials produced by stimulation of muscle nerves in the cat. Such field potentials were recorded in the intermediate zone of the fourth lumbar segment, where they display two distinct components, an early one from group I afferents and a later one from group II afferents. Both reflect EPSPs produced in interneurones in disynaptic pathways to motoneurones. Tizanidine strongly depressed potentials caused by group II afferents, while it had no effect or slightly facilitated potentials produced by group I afferents. In contrast, baclofen had inconsistent effects on the group II potentials; in some cases it caused a depression and in others it caused only an increase in the latency and time to peak, at doses that strongly and consistently depressed the group I potentials. These effects have been found after both local and systemic applications. The antispastic actions of tizanidine may therefore only be related to the depression of transmission from group II muscle afferents, while antispastic actions of baclofen may be secondary to the depression of any sensory fibres. Since tizanidine is as effective in depressing spasticity as baclofen, it is suggested that the enhancement in synaptic transmission from group II muscle afferents may play an important role in the development of exaggerated stretch reflexes in spastic patients.     

FR discrimination training reverses 6-hydroxydopamine-induced striatal dopamine depletion in a rat model of Lesch-Nyhan syndrome

Five-day-old rats received 6-hydroxydopamine (6-HD; 100 μ,g base) or vehicle intracisternally. Striatal and cortical dopamine (DA) and metabolite levels were then determined when animals were three or 8.5 months of age and the latter rats had been weight-reduced for 5.5 months. In the latter animals these determinations were made I month following 4.5 months of home-cage confinement (untrained animals) or of food-maintained fixed-ratio (FR) discrimination training involving either a single discrimination (performance animals) or incrementally more difficult discriminations. Striatal DA levels in 3-month-old and 8.5-month-old (untrained) 6-HD-treated rats were, respectively, only 3% and I I% of those in untrained vehicle-treated animals (controls). Despite such large depletions, striatal DA levels in 6-HD-treated performance rats were 3-fold higher than those in untrained age-matched 6-HD-treated rats (i.e., were 32% of values in controls) while those in incrementally trained 6-HD-treated animals were even higher (i.e., were 60% of control values). Related changes occurred in levels of most metabolites. However, in incrementally trained rats, striatal 3-methoxytyramine concentrations were 154% of control values. Cortical DA and metabolite levels were little affected by 6-HD treatment. The present results confirm and extend our earlier observations suggesting that reversal of ‘irreversible' neonatal 6-HD-induced striatal dopamine and metabolite depletion can be accomplished by environmental (training) manipulations in adult rats.     

Postnatal development of dendrites of relay neurons in the lateral geniculate nucleus of the marmoset (Callithrix jacchus): a quantitative Golgi study

Dendrites of multipolar relay neurons in the lateral geniculate nucleus of the marmoset (Callithrix jacchus), at various ages from birth to adulthood, were studied in rapid Golgi preparations. The dendrites were analyzed by means of three-dimensional computer reconstructions and decomposed into intermediate and terminal segments, both of which were further classified according to their centrifugal order. Measurements were made of the number of segments per dendrite, the total length of dendrites, and the mean length of intermediate and terminal segments. In adult marmosets, there are four stem dendrites on average per neuron, and each dendrite divides into a mean of 14 segments. Between birth and 6 weeks of age, the mean dendritic length doubles, mainly because of changes in terminal segments. There is a significant decrease in dendritic length into adulthood. The total number of stem dendrites does not change after birth, but during the first postnatal week dendrites lose distal segments, after which there is a significant increase in the number of segments of orders 3 to 7. The mean length of intermediate segments does not change with age, nor with order, whereas the length of terminal segments increases from 50 to 120 microns from birth to 6 weeks of age, and then decreases to the adult value of 80 microns. In conclusion, during the period of most rapid visual development, important morphological changes occur in geniculate relay-cell dendrites, involving essentially terminal segments. These observations correlate well with changes of geniculate volume and neuronal density.     

Synaptic proteins in frontal and control brain regions of rats after exposure to spatial problems

Synaptic proteins D1, D2, D3, synaptin and 14-3-2, as well as the glial protein glutamine synthetase, were measured by crossed immunoelectrophoresis in the anteromedial (prefrontal) cortex, occipital (visual) cortex and the anterior and posterior parts of the neostriatum of rats. The 3 experimental groups consisted of rats trained to criterion in a spatial delayed alternation, those run as yoked controls and, finally, rats kept in individual cages and not subjected to any training. Statistical analysis showed that two variables: behavioral procedures and brain regions, had a significant effect. Their interaction was also significant. Further analysis revealed that only in the prefrontal cortex of the yoked control animals was there a significant decrease of the synaptic membrane proteins D1, D2 and D3. Thus, particular behavioral treatment seems capable of affecting synapses in a specific ‘association’ cortical area. The change is more easily related to the amount of ‘work’ than to formation of ‘memory trace’ within the critical area.     

Synaptic potentials in smooth-muscle cells

Tests were carried out on the smooth-muscle cells (SMC) of the anococcygeus muscle of rats and rabbits by the double sucrose gap method with Krebs' solution containing tetraethylammonium (1 mmole/liter). Stimulation of a muscle strip from the anococcygeus of rats and rabbits by square pulses of maximal amplitude and short duration induced excitatory postsynaptic potentials (EPSPs) in rat and rabbit SMC and inhibitory postsynaptic potentials (IPSPs) in rabbit SMC. The amplitude of the postsynaptic potentials was a linear function of the membrane potential. Removal of chlorine ions from the external solution reduced the amplitude of EPSPs of SMC of the rabbit anococcygeus and shifted the reversal potential toward the sodium equilibrium potential. EPSP generation in SMC of the rabbit anococcygeus is evidently connected with an increase in membrane permeability to both sodium and chlorine ions.Department of Neuromuscular Physiology, A. A. Bogomolets Institute of Physiology, Academy of Sciences of the Ukrainian SSR, Kiev. (Presented by Academican of the Academy of Medical Sciences of the USSR N. N. Gorev.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 82, No. 8, pp. 913–916, August, 1976. Original article submitted July 11.     

Contrast and accommodation in amblyopia

Steady-state accommodation as a function of sinusoidal and square-wave grating contrast was measured in amblyopes. The amblyopic eyes exhibited reduced average response levels and required greater contrast to sustain accommodation than the fellow dominant eye or the eyes of visually-normal control subjects. Following therapy, accommodation in the amblyopic eye markedly improved. These results suggest: reduced accommodative controller gain, reduced stimulus effectiveness of target contrast, and considerable residual visual system plasticity with respect to the neurological control pathways of accommodation, in the amblyopic eye.     

Neurogenesis in the vomeronasal epithelium of adult garter snakes. 1. Degeneration of bipolar neurons and proliferation of undifferentiated cells following experimental vomeronasal axotomy

Postnatal cell proliferation, presumably for the purpose of neuronal replacement, was demonstrated in the vomeronasal epithelium of adult garter snakes using experimental vomeronasal axotomy. The luminal supporting cell layer of the epithelium did not undergo mitosis, nor necrosis, but exhibited some morphological modifications following axotomy. The bipolar layer underwent progressive irreversible degeneration following denervation. Degeneration of neurons progressed initially from alteration of cellular ultrastructure, to gross distortion of neuronal shapes followed by disintegration and disappearance of necrotic neurons. Maximal depletion of neurons occurred two weeks following surgery. The columnar epithelium at that time was characterized by the presence of a cell-depleted zone located between the luminal supporting cell layer and the basal, undifferentiated (Ud) cell layer. This cell-depleted zone occupied 70-80% of each degenerated cell column. Regeneration of axotomized neurons did not occur. The basally located, Ud cells exhibited no changes indicative of necrotic processes, but underwent active cell proliferation following axotomy. Changes in proliferative properties in the Ud cell layer were temporally related to the degeneration of the neuronal cell layer following nerve lesion. The Ud cell proliferation rate was slower than the rate of Bp cell degeneration. Proliferating Ud cells in the denervated epithelium may serve as the source of reconstituted vomeronasal bipolar neurons.     

Electrophysiological evidence for a PGE-mediated presynaptic control of acetylcholine output in the guinea-pig superior cervical ganglion

Intracellular recordings from single ganglion neurons show that 10⁻⁸−10⁻⁷M PGE₁ reversibly blocks synaptic transmission in isolated preparations of the guinea-pig superior cervical ganglion (SCG), when added to the superfusing medium. Neither resting potential nor membrane resistance of the impaled neurons appear to be affected by PGE₁. Quantal analyses of transmitter release demonstrate that the number of quanta liberated per volley is sharply reduced by PGE₁ treatment whereas the amplitude of the elementary event does not appear to be significantly changed.